Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis (Publication with Expression of Concern. See vol. 55, pg. 532, 2021)

被引:31
作者
Sun, Taitao [1 ]
Yu, Jian [2 ]
Han, Liang [3 ]
Tian, Shuo [4 ]
Xu, Bin [1 ]
Gong, Xianbin [1 ]
Zhao, Qiang [1 ]
Wang, Yang [5 ]
机构
[1] Jining 1 Peoples Hosp, Dept Orthoped, Jining, Peoples R China
[2] Heze Municipal Hosp, Dept Orthoped, Heze, Peoples R China
[3] Jining Med Univ, Affiliated Hosp, Dept Orthoped, Jining, Peoples R China
[4] Shandong Polytech Coll, Jining, Peoples R China
[5] Jilin Univ, China Japan Union Hosp, Dept Orthoped, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China
关键词
LncRNA RP11-445H22.4; MiR-301a; Cell viability; Apoptosis; Inflammatory injury; CXCR4; PROMOTES CELL-PROLIFERATION; B SIGNALING PATHWAY; COLORECTAL-CANCER; IN-VITRO; EXPRESSION; CXCR4; SUPPRESSES; DEGRADATION; CHONDROCYTE; INHIBITION;
D O I
10.1159/000487175
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Several long non-coding RNAs (lncRNAs) play vital roles in osteoarthritis (OA), whereas the role of lncRNA RP11-445H22.4 in OA remains unclear. The study aimed to investigate the effect of lncRNA RP11-445H22.4 on lipopolysaccharide (LPS)-induced cell viability, apoptosis and inflammatory injury of OA. Methods: The expression of RP11-445H22.4, miR-301a and CXCR4 in human cartilage ATDC5 cells were altered by transfection, and then cells were exposed to 5 mu g/ml LPS for 12 h. Then cell viability, apoptosis, apoptosis-related factors and inflammatory cytokines were analyzed by CCK-8, flow cytometry, western blot, RT-qPCR and ELISA, respectively. Dual-luciferase reporter assay was performed to assess the binging sites of RP11-445H22.4 and miR-301a. The signal pathways of NF-kappa B and MAPK/ERK were determined by western blot. Results: LPS reduced cell viability, increased apoptosis and stimulated release of IL-1 beta, IL-6, IL-8 and TNF-alpha. However, RP11-445H22.4 inhibition significantly rescued LPS-induced injuries by promoting cell viability, suppressing apoptosis and inflammatory cytokines secretions in ATDC5 cells. In addition, miR-301a directly bound to RP11-445H22.4, and suppression of miR-301a inversed the effects of RP11-445H22.4 inhibition. Furthermore, CXCR4 was a direct target of miR-301a, and CXCR4 silencing increased cell viability, decreased apoptosis and inflammatory cytokines secretions in LPS-treated ATDC5 cells. Besides, we found that CXCR4 silencing blocked LPS-activated NF-kappa B and MAPK/ERK pathways. Conclusions: The study indicated that lncRNA RP11-445H22.4-miR-301a-CXCR4 axis played an important role in cartilage ATDC5 cells and provided a theoretical basis of lncRNA RP11-445H22.4 in OA. (C) 2018 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:832 / 843
页数:12
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